Saxena M, Mukerji K G, Raj H G
Department of Botany, Vallabhbhai Patel Chest Institute, University of Delhi, India.
Biochem J. 1988 Sep 1;254(2):567-70. doi: 10.1042/bj2540567.
The presence of glutathione (GSH) S-transferase activity, using 1-chloro-2, 4-dinitrobenzene (CDNB) as a substrate, has been established in the cytosolic fraction of the toxigenic (aflatoxin producing) and nontoxigenic strains of Aspergillus flavus. Significant differences in the GSH S-transferase activity were observed between the toxigenic and non-toxigenic strains. A positive correlation has been demonstrated for the first time between aflatoxin formation and a biochemical parameter, namely GSH S-transferase activity. The evidence in support of A. flavus GSH S-transferase induction by endogenous aflatoxins is as follows: (i) the age-related production of aflatoxin follows the same pattern as the cytosolic GSH S-transferase activity profile; (ii) significantly higher enzyme activity was associated with mycelia of a toxigenic strain grown in medium supporting high aflatoxin production (sucrose-low-salts medium) while the enzyme activity was low in medium producing less aflatoxin (glucose-ammonium nitrate medium). The GSH S-transferase activity of the non-toxigenic strain was hardly affected by a change in the medium as it produces no aflatoxins; and (iii) the toxigenic strain demonstrated significantly higher apparent Vmax. with no change in Km as compared with the non-toxigenic strain. This indicates that the enzyme induction by endogenous aflatoxins is similar to the action of phenobarbitol and other inducing drugs (Kaplowitz et al., 1975).
已证实,以1-氯-2,4-二硝基苯(CDNB)为底物时,黄曲霉产毒菌株(产黄曲霉毒素)和非产毒菌株的胞质部分存在谷胱甘肽(GSH)S-转移酶活性。在产毒菌株和非产毒菌株之间观察到GSH S-转移酶活性存在显著差异。首次证明黄曲霉毒素形成与一个生化参数即GSH S-转移酶活性之间存在正相关。支持内源性黄曲霉毒素诱导黄曲霉GSH S-转移酶的证据如下:(i)黄曲霉毒素与年龄相关的产生模式与胞质GSH S-转移酶活性曲线相同;(ii)在支持高产黄曲霉毒素的培养基(蔗糖-低盐培养基)中生长的产毒菌株菌丝体的酶活性显著更高,而在产黄曲霉毒素较少的培养基(葡萄糖-硝酸铵培养基)中酶活性较低。非产毒菌株的GSH S-转移酶活性几乎不受培养基变化的影响,因为它不产生黄曲霉毒素;(iii)与非产毒菌株相比,产毒菌株表现出显著更高的表观Vmax,而Km没有变化。这表明内源性黄曲霉毒素对酶的诱导作用类似于苯巴比妥和其他诱导药物的作用(卡普洛维茨等人,1975年)。